INTRODUCTION
Lichen planopilaris (LPP), a variant of lichen planus, causes an inflammatory, cicatricial alopecia; the hallmarks of this disease include irregular patchy hair loss, destruction of follicular ostia, perifollicular erythema, and scaling. LPP includes three distinct clinical variants: classic LPP, frontal - brosing alopecia (FFA) and Graham-Little syndrome. Patients may experience intensely symptomatic affected areas with severe pruritus, scalp pain and tenderness as well as burning sensations.1 The goals of therapeutic treatment regimens for LPP patients are to minimize symptoms, and prevent progression of scarring hair loss. Conventional treatment consists of high potency topical corticosteroids and immunosuppressants, intralesional corticosteroids, topical minoxidil, and systemic anti-inflammatory agents such as doxycycline and hydroxychloroquine.2 Responses to available treatments can be unpredictable and are often inadequate. Currently, there are no consistently effective treatment options. The cause of LPP is unknown, but the histologic findings including dense lymphocytic in filtrate have led some to postulate this condition may be autoimmune.1 Recently, naltrexone an opioid antagonist with the greatest affinity for mu receptors, approved by the Food and Drug Administration for substance addiction treatment, has been suggested to be beneficial in treating autoimmune diseases. At low doses of less than 5mg daily, naltrexone acts paradoxically leading to an increase in endogenous opioids, among them β-endorphins which possess broad anti-inflammatory properties and orchestrate activity of T and B cells.3-5 In mice, administration of naltrexone following lipopolysaccharide-induced septic shock has been shown to block tumor necrosis factor-alpha production lending support to the assumption that this medication blocks inflammatory mediators.6 In addition, naltrexone alters the activity of macrophages causing a switch to the M1 type resulting in increased phagocytosis and processing of a greater number of antigens. Naltrexone has also been shown to produce an antagonistic effect on non-opioid receptors involved in the immune system including Toll-like receptor-4 found on cells such as macrophages and microglia, which may mediate both inflammation and neuropathic pain.8 Low-dose naltrexone has demonstrated efficacy in the adjunctive treatment of multiple autoimmune disorders including Crohn’s disease, and multiple sclerosis.9,10 In the dermatologic setting, naltrexone has been used effectively for patients with severe pruritus. Chronic pruritic disorders demonstrate downregulation of the μ-opioid receptor.11 Topically administered naltrexone has been shown to cause upregulation of the μ-opioid receptor, and provides better relief of pruritic symptoms relative to placebo.12 We hypothesized that low-dose naltrexone may be beneficial in patients with LPP to diminish inflammation and reduce itch, which many patients report is the most bothersome symptom. In this case series, we describe four patients with LPP including one patient with the FFA variant who were treated in a specialty Hair and Scalp Disorders Clinic located within a tertiary academic medical center (New York University Langone Medical Center) in New York, NY. These patients received 3 milligrams per day of naltrexone. Permission for this study was granted by the NYU Institutional Review Board (study: S16-01819).
CASE REPORTS
Case 1: 62-year-old male with more than a 5-year history of LPP. After 7 months of consecutive monthly intralesional
